Depression, diabetes and change in cognitive functioning: results from the Canadian Longitudinal study on Aging

Abstract Background Individuals who ultimately receive a diagnosis of dementia typically have an observable accelerated cognitive decline (ACD) many years prior to diagnosis. Depression in combination with diabetes is an emerging risk factor that is associated with cognitive problems. Using data from the Canadian Longitudinal Study on Aging, the objective of the present study was to investigate the longitudinal association between depression, diabetes, and cognitive decline in an elderly cohort. Methods Baseline and follow-up data from a population-based study in Canada were used. The sample consisted of 18161 adults between 45 and 85 years of age without diabetes. Cognitive functioning was assessed at baseline and after 4 years using six measures: the Rey Auditory Verbal Learning Test (RAVLT), the Mental Alternation Test (MAT), the Animal Fluency Test (AF), the Controlled Oral Word Association Test (COWAT), the Stroop Test, and the Prospective Memory Test. Depression was assessed using the CES-D10. Regression analysis was conducted to evaluate interactions between depression, diabetes and cognitive decline. Results The mean age of participants was 61 years. Participants with a comorbidity of depression and diabetes had an accelerated cognitive decline (g-factor) compared to those with depression without diabetes and those with diabetes without depression (regression coefficients ß=-0.145 (0.036), ß=-0.076 (0.011), and ß=-0.053 (0.021), respectively). Conclusions This study suggests that depression and diabetes might increase the risk of cognitive decline in a synergistic way.


Background:
Depression is a common co-morbidity in diabetes. The mechanisms underlying the association between depression and diabetes are poorly understood. Although risk factors, such as poor lifestyle behaviours, obesity, and stress have been identified, emerging evidence suggests that systemic inflammation may play an important role in the pathogenesis and recurrence of depression in people with diabetes. The aim of the present study was to evaluate if the inflammatory marker C-reactive protein (CRP) is associated with an increased risk of major depression episodes in people with type 2 diabetes.

Methods:
A prospective, community-based study was conducted in Quebec, Canada. Individuals were recruited from the CARTaGENE (CaG) cohort, a population-based survey of Quebec residents aged 40 to 69 years. Our sample included 719 individuals with type 2 diabetes and 1423 individuals without diabetes. Individuals were assessed at baseline and 5 years after baseline. Major depression disorders were assessed using a clinical interview (CIDI). Inflammatory markers were assessed from blood samples. Elevated CRP levels were defined as 3 mg/L.

Results:
Participants with both diabetes and elevated CRP levels had the highest risk of major depressive episodes (adjusted OR = 1.90, 95% CI 1.45, 2.50), compared to those without diabetes and without elevated CRP levels. The risk of major depressive episodes in individuals with diabetes without elevated CRP episodes was lower (adjusted OR = 1.21, 95% CI 0.85, 1.73) and similar to the risk of those without diabetes and elevated CRP levels (adjusted OR = 1.15, 95% CI 0.94, 1.39).

Discussion:
The study highlights the interaction between diabetes, inflammatory makers, and depression in a community sample. Early identification, monitoring, and management of elevated inflammation levels might be an important depression prevention strategy in people with type 2 diabetes.

Background:
Individuals who ultimately receive a diagnosis of dementia typically have an observable accelerated cognitive decline (ACD) many years prior to diagnosis. Depression in combination with diabetes is an emerging risk factor that is associated with cognitive problems. Using data from the Canadian Longitudinal Study on Aging, the objective of the present study was to investigate the longitudinal association between depression, diabetes, and cognitive decline in an elderly cohort.

Methods:
Baseline and follow-up data from a population-based study in Canada were used. The sample consisted of 18161 adults between 45 and 85 years of age without diabetes. Cognitive functioning was assessed at baseline and after 4 years using six measures: the Rey Auditory Verbal Learning Test (RAVLT), the Mental Alternation Test (MAT), the Animal Fluency Test (AF), the Controlled Oral Word Association Test (COWAT), the Stroop Test, and the Prospective Memory Test. Depression was assessed using the CES-D10. Regression analysis was conducted to evaluate interactions between depression, diabetes and cognitive decline.

Results:
The mean age of participants was 61 years. Participants with a comorbidity of depression and diabetes had an accelerated cognitive decline (g-factor) compared to those with depression without diabetes and those with diabetes without depression (regression coefficients ß = -0.145 (0.036), ß = -0.076 (0.011), and ß = -0.053 (0.021), respectively).

Conclusions:
This study suggests that depression and diabetes might increase the risk of cognitive decline in a synergistic way.
Abstract citation ID: ckac129.703 Time at home during the COVID-19 pandemic: a prospective examination of psychosocial health in people with and without type 2 diabetes using digital phenotyping

Introduction:
Societal restrictions due to COVID-19 have had a profound effect on our ability to connect with one another and limited our personal mobility. There is evidence that loneliness, social isolation, and psychological distress increased during restrictions for people with diabetes. Fluctuating restrictions provide a unique opportunity to utilise continuous GPS data from personal smartphones (digital phenotypes) to explore the relationship between time-at-home and psychosocial health for people with diabetes. This study aims to (1) describe the digital phenotypes of time-at-home during varying societal COVID-19 restrictions for people with and without type 2 diabetes and iii286 European Journal of Public Health, Volume 32 Supplement 3, 2022